12.12.12
Gilead Sciences has signed a definitive agreement to acquire YM BioSciences in transaction valued at approximately $510 million in cash. The transaction is expected to close in 1Q13.
YM’s lead drug candidate, CYT387, is an oral selective inhibitor of the Janus kinase (JAK) family, which has been implicated in a number of disorders including myeloproliferative diseases, inflammatory disorders and certain cancers. YM reported positive results from a Phase I/II trial of CYT387 in patients with myelofibrosis. Following the acquisition, Gilead plans to initiate a Phase III trial of CYT387 in myelofibrosis in 1H13.
“This acquisition represents an opportunity to add a complementary clinical program in the area of hematologic cancers to our growing oncology portfolio,” said Norbert W. Bischofberger, Ph.D., Gilead’s executive vice president, R&D and chief scientific officer. “Based on promising Phase II data, we believe CYT387 could provide important clinical benefit for patients with myelofibrosis, including potential improvements with regard to anemia and decreased dependence on blood transfusions. We look forward to advancing CYT387 into a Phase 3 study as quickly as possible and to exploring its potential in other myeloproliferative diseases with significant unmet medical need.”
YM’s lead drug candidate, CYT387, is an oral selective inhibitor of the Janus kinase (JAK) family, which has been implicated in a number of disorders including myeloproliferative diseases, inflammatory disorders and certain cancers. YM reported positive results from a Phase I/II trial of CYT387 in patients with myelofibrosis. Following the acquisition, Gilead plans to initiate a Phase III trial of CYT387 in myelofibrosis in 1H13.
“This acquisition represents an opportunity to add a complementary clinical program in the area of hematologic cancers to our growing oncology portfolio,” said Norbert W. Bischofberger, Ph.D., Gilead’s executive vice president, R&D and chief scientific officer. “Based on promising Phase II data, we believe CYT387 could provide important clinical benefit for patients with myelofibrosis, including potential improvements with regard to anemia and decreased dependence on blood transfusions. We look forward to advancing CYT387 into a Phase 3 study as quickly as possible and to exploring its potential in other myeloproliferative diseases with significant unmet medical need.”
